Key result
Schizophrenia was associated with significantly increased cardiac concentricity (d = 0.71) and reduced adiponectin levels (d = -0.69) compared to matched healthy controls, suggesting a non-hypertensive pathway to cardiac remodelling.
Why the study?
Cardiovascular diseases are the leading cause of death in schizophrenia, and patients show evidence of concentric cardiac remodelling, but the underlying molecular pathways remain unknown.
Do individuals with schizophrenia exhibit non-hypertensive pathways to concentric cardiac remodelling and adipose tissue dysfunction compared to matched healthy controls?
Case-Control (n=50)
No
Do individuals with schizophrenia exhibit non-hypertensive pathways to concentric cardiac remodelling and adipose tissue dysfunction compared to matched healthy controls?
Standardized Mean Difference: 0.71 (95% CI 0.12–1.3)
Absolute Event Rate: 1.05% vs 0.91%
p-value: p=0.01
Patients with schizophrenia exhibit non-hypertensive concentric cardiac remodeling and adipose tissue dysfunction, suggesting a dysmetabolic phenotype contributes to their excess cardiovascular risk.
May indicate non-hypertensive cardiac remodeling in schizophrenia; hypothesis-generating for dysmetabolic contributions to excess CV risk.
Cardiovascular diseases are the leading cause of death in schizophrenia. Patients with schizophrenia show evidence of concentric cardiac remodelling (CCR), defined as an increase in left-ventricular mass over end-diastolic volumes. CCR is a predictor of cardiac disease, but the molecular pathways leading to this in schizophrenia are unknown. We aimed to explore the relevance of hypertensive and non-hypertensive pathways to CCR and their potential molecular underpinnings in schizophrenia. In this multimodal case-control study, we collected cardiac and whole-body fat magnetic resonance imaging (MRI), clinical measures, and blood levels of several cardiometabolic biomarkers known to potentially cause CCR from individuals with schizophrenia, alongside healthy controls (HCs) matched for age, sex, ethnicity, and body surface area. Of the 50 participants, 34 (68%) were male. Participants with schizophrenia showed increases in cardiac concentricity (d = 0.71, 95% CI: 0.12, 1.30; p = 0.01), indicative of CCR, but showed no differences in overall content or regional distribution of adipose tissue compared to HCs. Despite the cardiac changes, participants with schizophrenia did not demonstrate activation of the hypertensive CCR pathway; however, they showed evidence of adipose dysfunction: adiponectin was reduced (d = -0.69, 95% CI: -1.28, -0.10; p = 0.02), with evidence of activation of downstream pathways, including hypertriglyceridemia, elevated C-reactive protein, fasting glucose, and alkaline phosphatase. In conclusion, people with schizophrenia showed adipose tissue dysfunction compared to body mass-matched HCs. The presence of non-hypertensive CCR and a dysmetabolic phenotype may contribute to excess cardiovascular risk in schizophrenia. If our results are confirmed, acting on this pathway could reduce cardiovascular risk and resultant life-years lost in people with schizophrenia.
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Osimo et al. (2021) conducted a case-control in Schizophrenia (n=50). Schizophrenia vs. Matched healthy controls was evaluated on Left ventricular concentricity (g/ml) (d = 0.71, 95% CI 0.12, 1.30, p=0.01). Schizophrenia was associated with significantly increased cardiac concentricity (d = 0.71) and reduced adiponectin levels (d = -0.69) compared to matched healthy controls, suggesting a non-hypertensive pathway to cardiac remodelling.
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